Shining a light on Parkinson’s disease
April is World Parkinson’s Awareness Month.
This is the first in a series of three articles, each looking at this condition through the lens of light — because most people (like me before researching this series) have no idea that Parkinson’s is, in large part, a disease of the eye.
This post reviews the basic mechanisms and overall implications for light and lighting. The second will focus on the role of light in prevention and management, and the third on implications for workplace design, as worldwide rates of Early Onset Parkinson’s disease tripled in just 30 years – Global burden of early-onset Parkinson’s disease, 1990–2021: results from the Global Burden of Disease Study 2021.
First things first: what is dementia, and where does Parkinson’s fit?
The word “dementia” is often used as if it were a diagnosis. But it isn’t.
Dementia is an umbrella term that describes a collection of symptoms — cognitive, functional, and behavioural — that can result from many different diseases, infections or injuries.
Parkinson’s disease, first described in 1817 by the English surgeon and political activist James Parkinson – An essay on the shaking palsy, together with a related condition called dementia with Lewy bodies, form the Lewy body dementias — the second most common cause of neurodegenerative dementia after Alzheimer’s disease – Jellinger K, “Parkinson’s Disease and Dementia with Lewy Bodies: One and the Same”.
So what’s that got to do with the eye?
Parkinson’s disease is caused by the progressive loss of dopamine-producing neurons in the substantia nigra, a region of the midbrain. Dopamine is also essential for the healthy function of the rods and intermediate signalling layers in the retina, including the melanopic system that signals to the body clock, mood regulation and attention systems in the brain. Retinal dopamine levels in people with Parkinsons levels fall to 40–60% below those of matched healthy controls – Decreased dopamine in the retinas of patients with Parkinson’s disease. The retina is not merely collateral damage; it is a central part of the pathological process – Dopaminergic Retinal Cell Loss and Visual Dysfunction in Parkinson Disease.
This retinal dopamine loss has measurable consequences for quality of life, mood and memory. It reduces contrast sensitivity — the ability to distinguish objects from their backgrounds when they are similar in brightness. It impairs light-dark adaptation, meaning that moving from a bright space into a darker one takes far longer and is far more disorienting than for a healthy person. It contributes to colour discrimination difficulties, particularly along the blue-yellow axis. And critically, visual deficits of this kind are detectable in early-stage and even pre-diagnostic PD, which means retinal examination is increasingly being explored as a biomarker for the disease – Retinal Changes in Parkinson’s Disease: A Non-invasive Biomarker for Early Diagnosis.
Hallucinations: the downstream consequence of visual pathway disruption
Visual hallucinations affect an estimated at 20–40% of people living with PD across the course of the disease, generated by a perfect storm of attenuated retinal signals, impaired contrast and spatial resolution, and downstream dysregulation in the cortical networks that normally predict and interpret sensory input. The brain simply ‘fills in the gaps’ – Hallucinations in Parkinson’s disease: new insights into mechanisms and treatments.
How does this compare with Alzheimer’s disease?
In Alzheimer’s disease (AD), the eye and retina are largely intact in the early stages. In these conditions, the problem lies in the way that visual information is interpreted by the parts of the brain that process spatial awareness, depth perception, and figure-ground discrimination. So a person may see perfectly well optically but cannot reliably read their environment: they may mistake a shadow for a step, or fail to distinguish a white plate from a white tablecloth.
In Parkinson’s, the problem begins earlier in the visual chain — in the retina itself. The eye is receiving the light, but its ability to process and transmit that signal is compromised. A person with PD in a dimly lit or low-contrast environment may be functionally unable to detect obstacles or read spatial cues, not because their brain is misinterpreting information, but because the retinal signal is attenuated at the source.
One important overlap is circadian disruption. In AD, the suprachiasmatic nucleus (SCN) — the brain’s master biological clock — atrophies significantly, which is why disrupted sleep and the characteristic ‘sundowning’ of late-day agitation are so prominent.
In PD, the circadian pathway is compromised differently: the melanopsin-containing intrinsically photosensitive retinal ganglion cells (ipRGCs), which are responsible for signalling daylight to the SCN and entraining the body clock, are directly affected with reduced density and degraded synaptic connections – a bidirectional hit – Circadian rhythm disruption: a potential trigger in Parkinson’s disease pathogenesis.
Disrupted circadian function is increasingly understood as both a symptom and a driver of neurodegeneration – Melanopsin Cell Dysfunction is Involved in Sleep Disruption in Parkinson’s Disease, Circadian clock dysfunction in Parkinson’s disease: mechanisms, consequences, and therapeutic strategy.
What does this mean for lighting design?
Illuminance levels need to be substantially higher than standard recommendations, while minimising glare. The retinal signal is attenuated, so someone living with PD needs more light. At the same time, the condition increases sensitivity to glare. So offering control, with diffuse, well-shielded luminaires; anti-reflective floor and surface finishes; and careful choice of luminance ratios between windows and interior surfaces are all essential – Management of Visual Dysfunction in Patients with Parkinson’s Disease.
Transition zones count. The impaired light-dark adaptation means that a sudden shift from a bright room to a dim stairwell (or stepping from a bright lobby to a dark garden path at night) creates a period of near-functional blindness that is disproportionately long in PD. Designing a gradual progression of luminance levels and offering a safe place to pause will give the visual system time to catch up, reducing stress and risk of falls.
Circadian lighting is a clinical intervention, not a luxury. For people with PD whose ipRGCs are functionally compromised, light levels in the morning need to be higher than current benchmarks to effectively anchor the body clock. Bright Light Therapy – at illuminance levels typically used for SAD lamps – been shown to improve sleep and subjective mood for people living with the condition – Adversities in childhood and young adulthood and incident cardiovascular diseases: a prospective cohort study, Supplemental ambient lighting intervention to improve sleep in Parkinson’s disease: A pilot trial, and may even improve visual function, too – Bright light therapy in Parkinson’s disease: a pilot study on visual pathway improvements. Bright mornings need to be balanced with softer, warmer lights in the evening and darkness at night. Alarmingly, artificial light at night is emerging as a risk factor for early-onset Parkinson’s disease alongside other degenerative diseases – Understanding light pollution: Recent advances on its health threats and regulations.
Parkinson’s disease is the fastest-growing neurodegenerative disease worldwide, with an estimated 5-10% of cases presenting between 21 and 50 years old – Alzheimer’s vs. Parkinson’s: A Comparison.
As lighting professionals, we can make a world of difference to the growing number of people in our community living with this condition through simple, thoughtful choices. And it doesn’t have to cost the earth.
Edible Easter experiment – measure the speed of light with chocolate in your microwave…
This video gives a great explanation of how standing waves work, the difference between wavelength and frequency – and a great excuse to tuck into some chocolate.
It explains how the distance between two melted patches on a large chocolate bar placed in a microwave (with the turntable removed) gives you half the length of the wave generated by your microwave. Double that to get a whole wavelength, then multiply that by the microwave’s frequency (found on the back of the machine).
You should get a number close to the speed of light – around 299,792,458 meters per second – although it will probably be a bit slower because the standard for the speed of light is measured in a vacuum.
One piece of homework I won’t mind doing over again!